BACKGROUND/AIMS: Infection of pancreatic necrosis is one of the leading cause of death in patients with severe necrotizing pancreatits. Because of high mortality rate up to 50%, immediate surgical debridement including pancreatectomy is recommended. However, early surgical treatment still showed high mortality rate and better treatment strategy is required. This study was conducted to evaluate the outcomes of early intensive non-surgical treatments in patients with infected necrotizing pancreatitis. METHODS: This study was based on retrospective analysis of 71 patients with acute severe necrotizing pancreatitis (APACHE II score>or=8, or Ranson's score>or=3, and pancreatic necrosis on CT scan), who were admitted to medical center during past 16 years. Infection of pancreatic necrosis was confirmed by fine needle aspiration, and early intensive medical treatments comprised of prophylactic antibiotics coverage, fluid resuscitation, organ preserving supportive measures, and percutaneous catheter drainage were carried out. RESULTS: Among the enrolled patients, infections were suspected in 46 patients, but fine needle aspirations were done only in 32 patients. In 21 patients, infections of necrotic tissue were confirmed by bacteriology, while other 11 patients showed no evidence of bacterial growth. Of 21 patients with infected necrosis, initial surgical interventions were performed in 2 patients, while initial medical treatments were performed in 19 patients. The success rate of medical treatment group in infected necrotizing pancreatitis was 79% (15/19). The mortality rate of medical treatment group and surgical treatment group was 5% (1/19) and 50% (1/2). CONCLUSIONS: Early intensive medical treatment seems to be a good therapeutic strategy, even if the infection has developed in pancreatic necrosis. Further prospective randomized studies are required to confirm this finding.
Bacterial Infections/diagnosis/*prevention & control ; Humans ; Pancreatitis, Acute Necrotizing/complications/diagnosis/*therapy ; Retrospective Studies ; Treatment Outcome

BACKGROUND/AIMS: Epigenetic silencing of DNA repair genes, O6-methylguanine-DNA methyltransferase (MGMT), hMLH1 and hMSH3, by promoter hypermethylation have been observed in various cancers. However, the relationship between hypermethylation of DNA mismatch repair genes and microsatellite instability (MSI) has not been studied in hepatocellular carcinoma (HCC) associated with cirrhosis. METHODS: We investigated the methylation pattern of CpG islands of 3 genes using methylation-specific PCR (MSP) and MSI in 40 patients with paired hepatocellular carcinoma and associated cirrhosis. RESULTS: hMSH3 and MGMT were the most methylated genes in both cirrhosis (70% and 68%, respectively) and HCC (75% and 73%, respectively). The methylation of hMLH1 was rarely found in both cirrhosis (8%) and HCC (5%). Gene promoters methylated in cirrhosis were also methylated in HCC with the exception of 9 cases found to be methylated either in cirrhosis or HCC. Of 40 cases of HCC associated with cirrhosis, three had MSI-positive phenotype in which two were MSI-low and one was MSI-high. One MSI-positive phenotype was present both in cirrhosis and in HCC, while two were only in HCC. There was no significant correlation between aberrant DNA methylation of mismatch repair genes and MSI status in HCC associated with cirrhosis. Immunohistochemical expressions of hMLH1, MGMT, and hMSH3 proteins were present in 16 (40%), 6 (15%), and 11 (28%) of 40 cases of HCC respectively. There was no significant correlaton between the aberrant DNA methylation of mismatch repair genes and clinical characteristics such as histological differentiation, postoperative recurrence and mortality. CONCLUSIONS: The methylation of MGMT and hMSH3 among DNA repair genes are frequent, but those of hMLH1 and MSI is very rare in both cirrhosis and HCC. There is no significant correlation between the methylation of DNA repair genes and clinical characteristics of HCC.
Adaptor Proteins, Signal Transducing/genetics ; Adult ; Aged ; Carcinoma, Hepatocellular/complications/diagnosis/*genetics ; *DNA Methylation ; DNA Modification Methylases/genetics ; *DNA Repair ; DNA Repair Enzymes/*genetics ; DNA-Binding Proteins/genetics ; Female ; Humans ; Liver Cirrhosis/complications/diagnosis/*genetics ; Liver Neoplasms/complications/diagnosis/*genetics ; Male ; *Microsatellite Instability ; Middle Aged ; Nuclear Proteins/genetics ; Tumor Suppressor Proteins/genetics

BACKGROUND/AIMS: Serum alpha-fetoprotein (AFP) is frequently used for the diagnosis of hepatocellular carcinoma (HCC). Most available data concerning AFP came from studies of patients with chronic hepatitis B or mixed etiologies. Studies concerning the diagnostic value of AFP for HCV-related liver cirrhosis (LC) are limited. We evaluated the factors influencing AFP elevation in the absence of HCC and analyzed the diagnostic value of serum AFP in HCC surveillance of HCV-related LC patients. METHODS: We enrolled 55 patients of HCV-related LC with HCC and 62 patients without HCC as a case-control study were analyzed. The sensitivity and specificity were calculated and the clinical and biochemical factors influencing serum AFP levels. RESULTS: The sensitivities and specificities of serum AFP for the detection of HCC in HCV-related LC were 72.7% and 59.7% for AFP> or =20 ng/mL, and 47.3% and 92.5% for AFP> or =100 ng/mL, respectively. Elevated serum AST was independently associated with elevated serum AFP level in HCV-related LC. In cases of AST< or =2 x upper limit of normal (ULN), the specificity of AFP> or =100 ng/mL for the diagnosis of HCC was 100%. However, in case of AST>2 x ULN, the specificity was 85.0% for AFP> or =100 ng/mL and 95.0% for AFP> or =200 ng/mL. CONCLUSIONS: Serum AST levels influence serum AFP level in HCV-related LC. In cases of AST< or =2 x ULN, AFP greater than 100 ng/mL highly indicates HCC in HCV-related LC, but not in case of AST>2 x ULN.
Aged ; Carcinoma, Hepatocellular/complications/*diagnosis/pathology ; Diagnosis, Differential ; Female ; Hepatitis C/*complications/immunology/virology ; Humans ; Liver Cirrhosis/*virology ; Liver Neoplasms/complications/*diagnosis/pathology ; Male ; Middle Aged ; Retrospective Studies ; Sensitivity and Specificity ; Tumor Markers, Biological/*blood ; alpha-Fetoproteins/*analysis

BACKGROUND/AIMS: Although erythrocyte sedimentation rate (ESR) is included as a laboratory parameter in Truelove and Witts' classification, C-reactive protein (CRP) is also used for severity assessment in ulcerative colitis (UC). Frequently, the discordance between ESR and CRP is observed in clinical practice. The aim of this study was to determine which parameter is more related with clinical activity in UC patients. METHODS: A total of 155 patients with UC were identified from January 2004 to March 2005. Their medical records were reviewed within these patients, a total of 541 assessments of disease activity were made. Correlation of clinical activity and laboratory tests were evaluated by Pearson's correlation coefficient. RESULTS: Pearson's correlation coefficients of ESR and CRP with clinical symptoms were 0.376 and 0.258, respectively. The correlation coefficient between ESR and CRP was 0.403 (p=0.000). A total of 131 (24.2%) assessments revealed discordance between ESR and CRP. When discordance occurred, the correlation coefficients with clinical symptoms were 0.338 for ESR (p=0.000) and 0.034 for CRP (p>0.01). Dividing discordant patients into high ESR/low CRP group and low ESR/high CRP group, the coefficients were 0.420 for ESR and 0.226 for CRP in high ESR/low CRP group, and 0.333 for ESR and 0.068 for CRP in low ESR/high CRP group. CONCLUSIONS: The correlation analysis indicates that ESR appears to be a more reliable laboratory parameter of disease activity than CRP in assessing the severity of UC. In particular, when the level of ESR and CRP is discordant, ESR is more useful in assessing the disease activity in UC patients.
*Blood Sedimentation ; C-Reactive Protein/*analysis ; Colitis, Ulcerative/blood/*diagnosis ; Humans ; Severity of Illness Index

BACKGROUND/AIMS: The clinical course of patients with inflammatory bowel disease (IBD) frequently leads to the use of immunosuppressants and immunomodulators. We investigated the risk of postoperative infection in patients with IBD undergoing elective bowel surgery and whether the use of corticosteroid (CS) and/or 6-mercaptopurine/ azathioprine (6-MP/AZA) before surgery was associated with the increased risk of postoperative infection. METHODS: Patients who were diagnosed as Crohn's disease (n=25) or ulcerative colitis (n=19) and underwent elective bowel surgery between 1986 and 2005 were identified. Medical records were retrospectively analyzed including age, sex, duration of disease, indication for surgery, duration of surgery, type of surgery, type of postoperative infection, admission period, usage of CS and 6-MP/AZA, and preoperative laboratory values. There were 27 patients receiving CS alone, 6 patients receiving 6-MP/AZA alone or with CS, and 16 patients receiving neither CS nor 6-MP/AZA. RESULTS: There were 17 postoperative infections (38.6%) among IBD patients who had undergone surgery and wound infection was the most common type of infection (76.5%). In IBD patients, patients receiving CS had higher postoperative infection rate than those patients receiving neither CS nor 6-MP/AZA (p=0.039). Patients receiving CS in conjunction with 6-MP/AZA did not have significantly higher postoperative infection rate than those with CS only (p=0.415). CONCLUSIONS: Preoperative use of CS in patients with IBD is associated with the increased risk of postoperative infections. Addition of 6-MP/AZA in patients receiving CS does not increase the risk of postoperative infections.
Colitis, Ulcerative/drug therapy/*surgery ; Crohn Disease/drug therapy/*surgery ; Humans ; Immunologic Factors/*adverse effects/therapeutic use ; Immunosuppressive Agents/*adverse effects/therapeutic use ; Infection/epidemiology/*etiology ; Postoperative Complications/epidemiology/*etiology ; Retrospective Studies

In acute injury, liver recovers completely without any scarring change or complication. However, large portion of liver is changed into fibrotic state by excessive production of extracellular matrix (ECM) under chronic injury. Excessive production of ECM results in hepatic fibrosis and repeated process of hepatic fibrosis progress into liver cirrhosis. Liver cirrhosis is an irreversible and terminal state of chronic liver disease and one of the major causes of death in Korea. To block the progression to liver cirrhosis, various studies in the field of virology and immunology have been proceeded. Recently, studies on the hepatic fibrogenesis have progressed with the development of molecular biology. Hepatic stellate cells (HSC) play a key role in the pathogenesis of hepatic fibrosis by producing ECM. The degree of hepatic fibrosis depends on the proliferation and activation of HSC and increased net production of collagen. Therefore, inhibition of HSC activation is one of the main ways to block the progression of hepatic fibrosis. Many kinds of factors such as oxidative stress, acetaldehyde, ascorbic acid, transforming growth factor-beta (TGF-beta) and carbon tetrachloride (CCl4) have been reported to activate HSC and stimulate collagen gene expression. Although there are no definite and effective antifibrogenic agents, possible candidates are antioxidants, interferon, retinoids such as beta-carotene, flavonoids, renin-angiotensin system inhibitors and peroxisome proliferator activated receptor-gamma (PPAR-gamma) agonists. We tried to evaluate the charateristics of HSC in order to develop agents that inhibit hepatic fibrogenesis.
Extracellular Matrix/*metabolism ; Fibrosis ; Humans ; Liver/blood supply/metabolism/*pathology ; Liver Cirrhosis/etiology/genetics/*metabolism

No abstract available.

No abstract available.

No abstract available.
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Helicobacter Infections/complications/drug therapy ; Helicobacter pylori ; Humans ; Peptic Ulcer/drug therapy/*etiology ; Recurrence ; Republic of Korea ; Risk Factors ; Smoking

This report describes a patient with hepatic congestion due to right heart failure mimicking liver tumor. The patient had a history of breast cancer and left total mastectomy 30 years ago, tricuspid valve regurgitation and tricuspid valve replacement 4 years ago. Three years ago, abdominal contrast-enhanced computed tomography (CT) was performed to evaluate inguinal hernia, which revealed multiple small hepatic nodules. After 1 year, the number and size of liver nodules were increased in CT scan. The patient underwent gun biopsy and histopathology revealed sinusoid enlargement. The patient recently had jaundice, abdominal distension, and peripheral edema. Liver dynamic CT scan was done to evaluate the palpable liver. The number and size of liver nodules were more increased in CT than 2 years ago. In magnetic resonance imaging (MRI), numerous variable sized ill-defined nodules replacing entire liver with progressing centripetal enhancement, which were suggestive of malignancy such as angiosarcoma, were noted. MRI finding suspects malignancy or hemangiosarcoma. Finally, the patient received repeated gun biopsy, and histopathology revealed findings compatible with hepatic congestion.
Biopsy, Needle ; Female ; Heart Failure/*complications ; Humans ; Liver Diseases/*diagnosis/etiology/pathology ; Liver Neoplasms/diagnosis ; Magnetic Resonance Imaging ; Middle Aged ; Tomography, X-Ray Computed